Anistreplase
An acylated inactive complex of streptokinase and human lysine-plasminogen. After injection, the acyl group is slowly hydrolyzed, producing an activator that converts plasminogen to plasmin, thereby initiating fibrinolysis. Its half-life is about 90 minutes compared to 5 minutes for TPA; (TISSUE PLASMINOGEN ACTIVATOR); 16 minutes for UROKINASE-TYPE PLASMINOGEN ACTIVATOR and 23 minutes for STREPTOKINASE. If treatment is initiated within 3 hours of onset of symptoms for acute myocardial infarction, the drug preserves myocardial tissue and left ventricular function and increases coronary artery patency. Bleeding complications are similar to other thrombolytic agents.
Thrombolytic Therapy
Streptokinase
Controlled Clinical Trials as Topic
Works about clinical trials involving one or more test treatments, at least one control treatment, specified outcome measures for evaluating the studied intervention, and a bias-free method for assigning patients to the test treatment. The treatment may be drugs, devices, or procedures studied for diagnostic, therapeutic, or prophylactic effectiveness. Control measures include placebos, active medicines, no-treatment, dosage forms and regimens, historical comparisons, etc. When randomization using mathematical techniques, such as the use of a random numbers table, is employed to assign patients to test or control treatments, the trials are characterized as RANDOMIZED CONTROLLED TRIALS AS TOPIC.
Myocardial Infarction
Thrombolytic therapy in Europe: current status. (1/39)
Thrombolytic therapy is a practical, effective approach to the management of acute myocardial infarction that is widely used in Europe today. Early European trials demonstrated a clear reduction in mortality in patients who received thrombolytic therapy compared with those given conventional treatment. The findings of experimental studies suggest that early reperfusion of the infarct-related artery reduces myocardial damage, which results in the preservation of left ventricular function and, in turn, may improve survival. Although tissue plasminogen activator (t-PA) has been shown to produce more rapid and complete reperfusion than streptokinase, two large-scale clinical trials in which t-PA was given as a standard 3- or 4-h infusion provided no evidence of a survival advantage with this agent. However, the accelerated t-PA regimen used in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) study was associated with a lower mortality than streptokinase or a combination of t-PA and streptokinase, thus lending support to the 'open artery' theory. Two recent studies conducted in Europe, the Grampian Region Early Anistreplase Trial (GREAT) and the European Myocardial Infarction Project (EMIP), have demonstrated the feasibility, safety, and efficacy of early thrombolytic therapy before admission to hospital. In GREAT, anistreplase (APSAC) was administered at home by general practitioners. In EMIP, this same agent was given by emergency medical personnel. In both studies, pre-hospital administration reduced the time between the onset of symptoms and initiation of thrombolysis and was associated with a lower mortality rate. Recent data from the European Cooperative Group Study show that the benefits of thrombolytic therapy are maintained for up to 5 years. Research continues in an effort to develop safer and more effective thrombolytic agents. Educational efforts to familiarize the public with the symptoms of myocardial infarction and the development of more rapid, efficient emergency response systems may also improve the outcome of thrombolytic therapy by shortening the time between symptom onset and thrombolytic drug administration. (+info)Monitoring of streptokinase resistance titre in acute myocardial infarction patients up to 30 months after giving streptokinase or anistreplase and related studies to measure specific antistreptokinase IgG. (2/39)
OBJECTIVE: To examine the induction of antistreptokinase antibodies after giving streptokinase or anistreplase to patients with acute myocardial infarction. DESIGN: Patients were randomly allocated to receive either 1.5 x 10(6) IU, streptokinase or 30U anistreplase in a double blind study. Blood samples were collected immediately before treatment and subsequently at intervals up to 30 months; plasma samples were assayed for streptokinase resistance titre (functional assay) and streptokinase binding by IgG (microradioimmunoassay). SETTING: Cardiology department in a general hospital. PATIENTS: 128 consecutive eligible patients. Samples were collected for up to one year according to a prospective design: a subsection of 47 patients was selected for intensive study over the first 14 days. After one year, all available patients (67) were sampled on one further occasion. RESULTS: Antibody responses to streptokinase and anistreplase were similar. Streptokinase resistance titres exceeded pretreatment concentrations five days after dosing, and values peaked at 14 days. By 12 months after dosing, 92% of resistance titres (n = 84) had returned to within the pretreatment range. Antistreptokinase IgG concentrations also exceeded baseline concentrations within five days and peaked at 14 days. Half of the individual values had returned to within the pretreatment range by 12 months (n = 84) and 89% by 30 months (n = 18). CONCLUSION: Although we cannot be sure of the clinical significance, because of the increased likelihood of resistance due to antistreptokinase antibody, streptokinase and anistreplase may not be effective if administered more than five days after an earlier dose of streptokinase or anistreplase, particularly between five days and 12 months, and increased antistreptokinase antibody may increase the risk of allergic-type reactions. (+info)Feasibility, safety, and efficacy of domiciliary thrombolysis by general practitioners: Grampian region early anistreplase trial. GREAT Group. (3/39)
OBJECTIVE: To assess the feasibility, safety, and efficacy of domiciliary thrombolysis by general practitioners. DESIGN: Randomised double blind parallel group trial of anistreplase 30 units intravenously and placebo given either at home or in hospital. SETTING: 29 rural practices in Grampian admitting patients to teaching hospitals in Aberdeen (average distance 36 (range 16-62) miles). PATIENTS: 311 patients with suspected acute myocardial infarction and no contraindications to thrombolytic therapy seen at home within four hours of onset of symptoms. MAIN OUTCOME MEASURES: Time saving, adverse events, Q wave infarction, left ventricular function. RESULTS: Anistreplase was administered at home 101 minutes after onset of symptoms, while anistreplase was given in hospital 240 minutes after onset of symptoms (median times). Adverse events after thrombolysis were infrequent and, apart from cardiac arrest, not a serious problem when they occurred in the community: seven of 13 patients were resuscitated after cardiac arrest out of hospital. By three months after trial entry the relative reduction of deaths from all causes in patients given thrombolytic therapy at home was 49% (13/163 (8.0%) v 23/148 (15.5%); difference -7.6% (95% confidence interval -14.7% to -0.4%), p = 0.04). Full thickness Q wave infarction was less common in patients with confirmed infarction receiving treatment at home (65/122 (53.3%) v 76/112 (67.9%); difference -14.6% (95% confidence interval -27.0% to -2.2%), p = 0.02). CONCLUSIONS: General practitioners provided rapid pre-hospital coronary care of a high standard. Compared with later administration in hospital, giving anistreplase at home resulted in reduction in mortality, fewer cardiac arrests, fewer Q wave infarcts, and better left ventricular function. Benefits were most marked where thrombolytic therapy was administered within two hours of the onset of symptoms. (+info)Oesophageal dissection after thrombolytic treatment for myocardial infarction. (4/39)
A 62 year old woman admitted with a history suggesting acute myocardial infarction had thrombolytic treatment with anisoylated plasminogen-streptokinase activator complex, which resulted in submucosal haemorrhage in the oesophagus; this caused dissection of the wall of the oesophagus and complete dysphagia. The haematoma resolved spontaneously, leaving behind a diverticulum, with reduced peristalsis and delayed emptying but no obstruction. (+info)The pharmacological modulation of thrombin-induced cerebral thromboembolism in the rabbit. (5/39)
1. Intracarotid (i.c.) administration of thrombin induced a marked accumulation of 111indium-labelled platelets and 125I-labelled fibrinogen within the cranial vasculature of anaesthetized rabbits. 2. Thrombin (100 iu kg-1, i.c.) - induced platelet accumulation was completely abolished by pretreatment with desulphatohirudin (CGP 39393; 1 mg kg-1 i.c., 1 min prior to thrombin). Administration of CGP 39393 1 or 20 min after thrombin produced a significant reduction in platelet accumulation. 3. Intravenous (i.v.) administration of the platelet activating factor (PAF) receptor antagonist BN 52021 (10 mg kg-1) 5 min prior to thrombin (100 iu kg-1, i.c.) had no effect on platelet accumulation. 4. An inhibitor of NO biosynthesis, L-NG-nitro arginine methyl ester (L-NAME; 100 mg kg-1, i.c.), had no significant effect on the cranial platelet accumulation response to thrombin (10 iu kg-1, i.c.) when administered 5 min prior to thrombin. 5. Defibrotide (32 or 64 mg kg-1 bolus i.c. followed by 32 or 64 mg kg-1 h-1, i.c., infusion for 45 min) treatment begun 20 min after thrombin (100 iu kg-1, i.c.) did not significantly modify the cranial platelet accumulation response. 6. Cranial platelet accumulation induced by thrombin (100 iu kg-1, i.c.) was significantly reversed by the fibrinolytic drugs urokinase (20 iu kg-1, i.c., infusion for 45 min), anisoylated plasminogen streptokinase activator complex (APSAC) (200 micrograms kg-1, i.v. bolus) or recombinant tissue plasminogen activator (rt-PA; 100 micrograms kg-1, i.c. bolus followed by 20 micrograms kg-1 min-1, i.c., infusion for 45 min) administered 20 min after thrombin.8. These results suggest that neither endogenous PAF nor NO modulate thrombin-induced intracranial platelet accumulation in the rabbit. However, fibrin deposition appears to play an important role as shown by the ability of fibrinolytic agents to reverse platelet and fibrinogen accumulation induced by i.c. thrombin. (+info)Clinical and economic outcomes in thrombolytic treatment of peripheral arterial occlusive disease and deep venous thrombosis. (6/39)
PURPOSE: Over the past 2 decades the use of thrombolytic therapy in the management of peripheral occlusive diseases, most notably peripheral arterial occlusion (PAO) and deep venous thrombosis (DVT), has become an accepted and potentially preferable alternative to surgery. We examined the period when urokinase was in short supply and subsequently unavailable, to explore potential differences in clinical outcome and economic effect between urokinase and recombinant tissue plasminogen activator (rt-PA). MATERIAL AND METHODS: Data were obtained from the Premier Perspective Database, a broad clinical database that contains information on inpatient medical practices and resource use. The study population included all patients hospitalized in 1999 and 2000 with a primary or secondary diagnosis of PAO or DVT. Incidence was calculated for common adverse events, including bleeding complications, intracranial hemorrhage, amputation, and death. Cost data were also abstracted from the database, and are expressed as mean +/- SD. RESULTS: Demographic variables were similar in the urokinase and rt-PA groups. The rate of bleeding complications was similar in the urokinase and rt-PA groups. There were no intracranial hemorrhages in the urokinase group, compared with a rate of 1.5% in the rt-PA PAO group (P = .087) and 1.9% in the rt-PA DVT group (P = .175). The in-hospital mortality rate was lower in the urokinase-treated PAO subgroup (3.6% vs 8.5%; P = .026), but a similar finding in the DVT subgroup did not achieve statistical significance (4% vs 9.8%; P = .069). While pharmacy costs were greater in the urokinase-treated group (US 5472 dollars +/- US 5579 dollars vs US 3644 dollars +/- US 6009 dollars, P < .001; PAO subgroup, US 11,070 dollars +/- US 15,409 dollars vs US 6150 dollars +/- US 12,398 dollars, P = .003), overall hospital costs did not differ significantly between the 2 groups. This finding appears to be explained by a shorter hospital stay and reduced room and board costs in the urokinase-treated group. CONCLUSION: There were significant differences in outcome in patients with PAO and DVT who received treatment with urokinase and rt-PA. While pharmacy costs were significantly greater when urokinase was used, reduction in length of stay accounted for similar total hospital costs compared with rt-PA. These findings must be considered in the context of the retrospective nature of the analysis and the potential to use dosing regimens that differ from those in this study. (+info)Serum myoglobin and creatine kinase enzymes in acute myocardial infarction treated with Anistreplase. (7/39)
AIMS: To compare plasma myoglobin concentration and cardiac enzyme activity with electrocardiographic (ECG) changes in two groups of patients (reperfused and non-reperfused) participating in a placebo-controlled randomised double blind trial of treatment of myocardial infarction (MI) with intravenous thrombolytic therapy (Anistreplase). METHODS: Twenty two patients with confirmed MI obeying strict inclusion and exclusion criteria were studied. Plasma myoglobin was measured by radioimmunoassay and creatine kinase enzyme (CK and CKMB) by NAC activated and NAC activated/immunoinhibition methods respectively in all patients before and at frequent intervals after injection of Anistreplase or placebo. Patients were divided into reperfused (R) and non-reperfused (NR) groups on the basis of ECG criteria. Reperfusion was diagnosed if the measured ST segment elevation fell by greater than or equal to 50% at 2 hours post dosing. RESULTS: The time to peak (TTP) myoglobin was significantly less in the R group compared with the NR group but there was considerable overlap in the range of values. The area under the enzyme time curves (AUCs) and summed ST segment epsilon ST elevations were significantly smaller in the R compared with the NR group. CONCLUSIONS: Although TTP myoglobin results were significantly lower in the R group, TTP myoglobin will probably not be useful as an non-invasive indicator of reperfusion because of the overlap in values between the two groups. The significant reduction in the AUC and epsilon ST only in the R group suggests decreased infarct size. However, in this small preliminary study reperfusion did not occur more frequently with Anistreplase than without. (+info)Evaluation of thrombolytic and systemic effects of the novel recombinant plasminogen activator BM 06.022 compared with alteplase, anistreplase, streptokinase and urokinase in a canine model of coronary artery thrombosis. (8/39)
The thrombolytic and systemic effects of BM 06.022 were evaluated and compared with those of alteplase, anistreplase, streptokinase and urokinase in a canine model of coronary artery thrombosis. BM 06.022 consists of the kringle-2 and protease domains of human tissue plasminogen activator (t-PA) and is unglycosylated because of its expression in Escherichia coli cells. Thrombus formation in anesthetized open chest dogs was induced by electrical injury to the intimal surface of the left circumflex coronary artery at a high level site of obstruction. In heparinized dogs, none of six vehicle-treated animals exhibited reperfusion. Reperfusion was achieved in four of six dogs at 18.3 +/- 6 min after intravenous bolus injection of 140 kU/kg (0.24 mg/kg) of BM 06.022, whereas four of six dogs exhibited reperfusion later (p less than 0.05) at 76.5 +/- 16.1 min during infusion of 1.33 mg/kg of alteplase (0.13 mg/kg as initial bolus injection, followed by 0.66 mg/kg over 1 h and 0.53 mg/kg over 2 h). Significantly later (p less than 0.05) reperfusion than that achieved with BM 06.022 was achieved in five of six dogs at 57.8 +/- 12.1 min after intravenous injection of 0.4 U/kg of anistreplase. Streptokinase (21,000 IU/kg over 60 min) and urokinase (20,000 IU/kg as an intravenous bolus injection, followed by 20,000 IU/kg over 89 min) each induced reperfusion in three of six dogs but at 67 +/- 12 and 84.3 +/- 17.1 min (p less than 0.05 vs. BM 06.022), respectively.(ABSTRACT TRUNCATED AT 250 WORDS) (+info)Drug eruptions and isotypic antibody responses to streptokinase after infusions of anisoylated plasminogen-streptokinase...
ISIS-3: a randomised comparison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin plus heparin vs...
Does thrombolysis in myocardial infarction (TIMI) perfusion grade 2 represent a mostly patent artery or a mostly occluded...
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Anistreplase
... is a thrombolytic drug. It is also known as anisoylated plasminogen streptokinase activator complex (APSAC). As a ... Anistreplase is used to treat blood clots in emergency situations such as myocardial infarction. Early treatment gives better ... Anistreplase is a complex of purified human plasminogen and bacterial streptokinase that has been acylated to protect the ... Grampion Region Early Anistreplase Trial (GREAT)". J Epidemiol Community Health. 47 (5): 377-381. doi:10.1136/jech.47.5.377. ...
Fibrinolysis
Anistreplase Desmoteplase Streptokinase Nattokinase Lumbrokinase Serrapeptase Papain DNase Bromelain Honokiol Dugdale, David et ...
Acute limb ischaemia
More recently, drugs such as tissue plasminogen activator, urokinase, and anistreplase have been used in their place. ...
APSAC
... anistreplase) This disambiguation page lists articles associated with the title APSAC. If an internal link led you here, you ...
List of MeSH codes (D12.776.124)
... anistreplase MeSH D12.776.124.125.662.537.900 - streptodornase and streptokinase MeSH D12.776.124.125.662.768 - tissue ...
List of drugs: An-Ap
... anistreplase (INN) anitrazafen (INN) anivamersen (USAN, INN) Anodynos-DHC Anolor 300 Anoquan anpirtoline (INN) anrukinzumab ( ...
Beecham Group
... anistreplase) Engerix-B (hepatitis B vaccine) Floxapen (flucloxacillin) granisetron Havrix (hepatitis A vaccine) Orbenin ( ...
List of MeSH codes (D08)
... anistreplase MeSH D08.811.277.656.300.775.900 - streptodornase and streptokinase MeSH D08.811.277.656.350 - exopeptidases MeSH ... anistreplase MeSH D08.811.277.656.300.760.640 - proprotein convertase 1 MeSH D08.811.277.656.300.760.646 - proprotein ...
Thrombolysis
Tenecteplase Anistreplase (Eminase) In people who receive thrombolytic therapy delivered through a catheter, there is a risk of ...
International Studies of Infarct Survival
... and anistreplase to each other, and also compared the anticoagulant heparin to no heparin. All patients were also given aspirin ... a randomised comparison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin plus heparin vs aspirin ...
ATC code B01
... combinations with proton pump inhibitors B01AD01 Streptokinase B01AD02 Alteplase B01AD03 Anistreplase B01AD04 Urokinase B01AD05 ...
ANISTREPLASE - INJECTION (Eminase) side effects, medical uses, and drug interactions.
Read more about the prescription drug ANISTREPLASE - INJECTION. ... anistreplase-injection, Eminase. The display and use of drug ... Consumer information about the medication ANISTREPLASE - INJECTION (Eminase), includes side effects, drug interactions, ... GENERIC NAME: ANISTREPLASE - INJECTION (an-ISS-treh-plays). BRAND NAME(S): Eminase. Medication Uses , How To Use , Side Effects ...
Thrombolytics and Thrombolytic Therapy
Thrombolytic Therapy: Background, Thrombolytic Agents, Thrombolytic Therapy for Acute Myocardial Infarction
APSAC (anistreplase) is a complex of streptokinase and plasminogen that does not require free circulating plasminogen to be ... Like streptokinase, anistreplase does not distinguish between fibrin-bound and circulating plasminogen; consequently, it too ... The adult dose of APSAC (anistreplase) for AMI is 30 U given IV over 2-5 minutes. ...
Thrombolytic Therapy: Background, Thrombolytic Agents, Thrombolytic Therapy for Acute Myocardial Infarction
APSAC (anistreplase) is a complex of streptokinase and plasminogen that does not require free circulating plasminogen to be ... Like streptokinase, anistreplase does not distinguish between fibrin-bound and circulating plasminogen; consequently, it too ... The adult dose of APSAC (anistreplase) for AMI is 30 U given IV over 2-5 minutes. ...
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Thrombolytic Therapy: Background, Thrombolytic Agents, Thrombolytic Therapy for Acute Myocardial Infarction
APSAC (anistreplase) is a complex of streptokinase and plasminogen that does not require free circulating plasminogen to be ... Like streptokinase, anistreplase does not distinguish between fibrin-bound and circulating plasminogen; consequently, it too ... The adult dose of APSAC (anistreplase) for AMI is 30 U given IV over 2-5 minutes. ...
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Dowling, R. J. O., Sparano, J. A., Goodwin, P. J., Bidard, F. C., Cescon, D. W., Chandarlapaty, S., Deasy, J. O., Dowsett, M., Gray, R. J., Henry, N. L., Meric-Bernstam, F., Perlmutter, J., Sledge, G. W., Thorat, M. A., Bratman, S. V., Carey, L. A., Chang, M. C., DeMichele, A., Ennis, M., Jerzak, K. J., & 12 othersKorde, L. A., Lohmann, A. E., Mamounas, E. P., Parulekar, W. R., Regan, M. M., Schramek, D., Stambolic, V., Whelan, T. J., Wolff, A. C., Woodgett, J. R., Kalinsky, K. & Hayes, D. F., Dec 1 2019, In: JNCI Cancer Spectrum. 3, 4, pkz049.. Research output: Contribution to journal › Review article › peer-review ...
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Fibrinolytic System
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Warfarin
In the early 1920s, there was an outbreak of a previously unrecognized cattle disease in the northern United States and Canada. Cattle were haemorrhaging after minor procedures and on some occasions, spontaneously.[82] For example, 21 out of 22 cows died after dehorning and 12 out of 25 bulls died after castration. All of these animals had bled to death.[83]. In 1921, Frank Schofield, a Canadian veterinary pathologist, determined that the cattle were ingesting moldy silage made from sweet clover, and that this was functioning as a potent anticoagulant.[82] Only spoiled hay made from sweet clover (grown in northern states of the USA and in Canada since the turn of the century) produced the disease.[84] Schofield separated good clover stalks and damaged clover stalks from the same hay mow, and fed each to a different rabbit. The rabbit that had ingested the good stalks remained well, but the rabbit that had ingested the damaged stalks died from a haemorrhagic illness. A duplicate experiment with a ...
Streptokinase1
- The DDDs of streptokinase, alteplase, anistreplase and reteplase are based on thrombolytic treatment in connection with acute myocardial infarction. (whocc.no)